It is estimated that there are up to 8,000 distinct languages spoken around the world today. At birth, the human mind is capable of learning and understanding any of these languages; an impressive feat given how uniquely complex they are. The fact that humans are able to understand and communicate with one another in such a way that even our closest primate relatives cannot has long been supposed to be the result of some sort of genetic distinction separating us from the rest of the animal kingdom.
In 2002, scientists believed they had found this genetic distinction in the form of a gene called FOXP2. Their early studies suggested that FOXP2 was linked to the development of language in humans, and in humans’ ability to manipulate the brain, lungs, and vocal chords to make the complicated suite of sounds and movements resulting in speech.
However, the expression of FOXP2 in humans – and its presence in other species – is anything but simple. Research has revealed that FOXP2 isn’t expressed just in the brain, but in a host of other tissues and organs throughout the body. Moreover, FOXP2 isn’t unique to humans, but is found in many species, from chimpanzees to field mice. It’s the version of FOXP2 we humans carry that is distinct from those of other species. So it is the differences in FOXP2 across species that has been at the heart of scientific research into the origins of complex language.
A few years after the FOXP2 gene’s possible role in promoting complex language skills was announced in 2002, scientists analyzing ancient DNA extracted from Neanderthals, our closest fossil ancestors, found that they had the same version of FOXP2 as humans. This discovery was revolutionary, as it meant that humans may not have been the first species capable of complex speech and language. It also pushed back the appearance of this version of FOXP2 to at least 350,000 years ago.
Recently, the focus of genetic research into FOXP2 has focused on the specific role FOXP2 plays in our language ability. Was it involved in enhancing our cognitive abilities? Our motor skills? Our breathing patterns? The results of scientists’ most recent effort to uncover the answers to these questions are in the May 29th issue of Cell, in a paper published by researchers from the Max-Planck Institute of Evolutionary Anthropology.
In order to advance our understanding of FOXP2, the scientists chose to examine its expression in mice, a surprisingly strong model for many human biological systems. The chief difference in FOXP2 between humans and many other species such as mice boils down to two changes in the gene. At some point in human prehistory, these changes arose and quickly became universal in the FOXP2 of humans.
To see what effect those changes might have had, the Max Planck scientists altered the copies of FOXP2 in mice to be identical to the copies of FOXP2 in humans. They then examined any changes that took place surrounding the cognition and vocal skills of the genetically altered mice, to see how they might be affected by the supposedly advanced copy of FOXP2. And, while the linguistic skills of the mice failed to rival our own, the scientists did see some surprising changes. First, they found that the altered mice showed changes in their brain circuitry that bore some similarity to that of humans. And perhaps most intriguing, the altered mice had distinct ultrasonic vocalizations that differed from their unmodified brethren. Ultrasonic vocalizations, sometimes referred to as chirps or squeaks, are used by mice to communicate to each other, such as to warn of a predator. When the young altered mice were separated from their mothers, something that usually elicits many such squeaks, they emitted ultrasonic vocalizations that were distinctly different in intensity and frequency than their counterparts. The authors argue that the altered FOXP2 in the mice was influencing the type of squeaks that they were making when separated from their mothers. And the scientists therefore believe there is some kind of connection to language development.
But what does all this mean to humans? The past several years of research into FOXP2 has revealed that human patients who carry at least one non-functional version of the gene (i.e., the version of the gene found in species other than humans) have problems producing the facial movements necessary to form words. It had been thought that part of the function of FOXP2 in humans was to develop motor control needed to articulate our mouths, vocal chords, and esophagus to produce complex language. Many experts have also proposed that FOXP2 in humans plays a role in the development of both the lungs and the esophagus – both of which are vital to speech. This most recent study shows that by simply tweaking FOXP2 in mice, we see a noticeable change in how they communicate.
Clearly, there is much more work to be done and many more questions to be answered. In the future, these researchers envision going even further to understand exactly how FOXP2 influences our ability to communicate with each other. Their next goal? To understand the exact mechanics behind the version of FOXP2 found in humans, so that they can finally piece together its importance in giving us the power of speech.